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Periodontology 2000 Feb 2021Interspecies interactions are key determinants in biofilm behavior, ecology, and architecture. The cellular responses of microorganisms to each other at transcriptional,... (Review)
Review
Interspecies interactions are key determinants in biofilm behavior, ecology, and architecture. The cellular responses of microorganisms to each other at transcriptional, proteomic, and metabolomic levels ultimately determine the characteristics of biofilm and the corresponding implications for health and disease. Advances in omics technologies have revolutionized our understanding of microbial community composition and their activities as a whole. Large-scale analyses of the complex interaction between the many microbial species residing within a biofilm, however, are currently still hampered by technical and bioinformatics challenges. Thus, studies of interspecies interactions have largely focused on the transcriptional and proteomic changes that occur during the contact of a few prominent species, such as Porphyromonas gingivalis, Streptococcus mutans, Candida albicans, and a few others, with selected partner species. Expansion of available tools is necessary to grow the revealing, albeit limited, insight these studies have provided into a profound understanding of the nature of individual microbial responses to the presence of others. This will allow us to answer important questions including: Which intermicrobial interactions orchestrate the myriad of cooperative, synergistic, antagonistic, manipulative, and other types of relationships and activities in the complex biofilm environment, and what are the implications for oral health and disease?
Topics: Biofilms; Candida albicans; Humans; Porphyromonas gingivalis; Proteomics; Streptococcus mutans
PubMed: 33226675
DOI: 10.1111/prd.12354 -
Odontology Jan 2022Porphyromonas gingivalis, a Gram-negative anaerobic bacillus present in periodontal disease, is considered one of the major pathogens in periodontitis. A literature... (Review)
Review
Porphyromonas gingivalis, a Gram-negative anaerobic bacillus present in periodontal disease, is considered one of the major pathogens in periodontitis. A literature search for English original studies, case series and review articles published up to December 2019 was performed using the MEDLINE, PubMed and GoogleScholar databases, with the search terms "Porphyromonas gingivalis" AND the potentially associated condition or systemic disease Abstracts and full text articles were used to make a review of published research literature on P. gingivalis outside the oral cavity. The main points of interest of this narrative review were: (i) a potential direct action of the bacterium and not the systemic effects of the inflammatory acute-phase response induced by the periodontitis, (ii) the presence of the bacterium (viable or not) in the organ, or (iii) the presence of its virulence factors. Virulence factors (gingipains, capsule, fimbriae, hemagglutinins, lipopolysaccharide, hemolysin, iron uptake transporters, toxic outer membrane blebs/vesicles, and DNA) associated with P. gingivalis can deregulate certain functions in humans, particularly host immune systems, and cause various local and systemic pathologies. The most recent studies linking P. gingivalis to systemic diseases were discussed, remembering particularly the molecular mechanisms involved in different infections, including cerebral, cardiovascular, pulmonary, bone, digestive and peri-natal infections. Recent involvement of P. gingivalis in neurological diseases has been demonstrated. P. gingivalis modulates cellular homeostasis and increases markers of inflammation. It is also a factor in the oxidative stress involved in beta-amyloid production.
Topics: Adhesins, Bacterial; Gingipain Cysteine Endopeptidases; Humans; Periodontitis; Porphyromonas gingivalis
PubMed: 34410562
DOI: 10.1007/s10266-021-00647-8 -
International Endodontic Journal Oct 2023Angiogenesis contributes to the development of apical periodontitis, periodontitis, and other oral pathologies; however, it remains unclear how this process is...
AIM
Angiogenesis contributes to the development of apical periodontitis, periodontitis, and other oral pathologies; however, it remains unclear how this process is triggered. The aim was to evaluate whether lipopolysaccharide (LPS) from Porphyromonas endodontalis and Porphyromonas gingivalis induced angiogenesis-related effects in vitro via TLR2 and TLR4.
METHODOLOGY
Porphyromonas endodontalis LPS (ATCC 35406 and clinical isolate) was purified with TRIzol, whereas P. gingivalis LPS was obtained commercially. The effects of the different LPS (24 h) in endothelial cell migration were analysed by Transwell assays, following quantification in an optical microscope (40×). The effects of LPS on FAK Y397 phosphorylation were assessed by Western blotting. Angiogenesis in vitro was determined in an endothelial tube formation assay (14 h) in Matrigel in the absence or presence of either LPS. IL-6 and VEGF-A levels were determined in cell supernatants, following 24 h treatment with LPS, and measured in multiplex bead immunoassay. The involvement of TLR2 and TLR4 was assessed with blocking antibodies. The statistical analysis was performed using STATA 12® (StataCorp LP).
RESULTS
The results revealed that P. endodontalis LPS, but not P. gingivalis LPS, stimulated endothelial cell migration. Pre-treatment with anti-TLR2 and anti-TLR4 antibodies prevented P. endodontalis LPS-induced cell migration. P. endodontalis LPS promoted FAK phosphorylation on Y397, as observed by an increased p-FAK/FAK ratio. Both P. gingivalis and P. endodontalis LPS (ATCC 35406) induced endothelial tube formation in a TLR-2 and -4-dependent manner, as shown by using blocking antibodies, however, only TLR2 blocking decreased tube formation induced by P. endodontalis (clinical isolate). Moreover, all LPS induced IL-6 and VEGF-A synthesis in endothelial cells. TLR2 and TLR4 were required for IL-6 induction by P. endodontalis LPS (ATCC 35406), while only TLR4 was involved in IL-6 secretion by the other LPS. Finally, VEGF-A synthesis did not require TLR signalling.
CONCLUSION
Porphyromonas endodontalis and P. gingivalis LPS induced angiogenesis via TLR2 and TLR4. Collectively, these data contribute to understanding the role of LPS from Porphyromonas spp. in angiogenesis and TLR involvement.
Topics: Lipopolysaccharides; Toll-Like Receptor 2; Porphyromonas gingivalis; Porphyromonas endodontalis; Vascular Endothelial Growth Factor A; Endothelial Cells; Antibodies, Blocking; Interleukin-6; Toll-Like Receptor 4
PubMed: 37461231
DOI: 10.1111/iej.13957 -
Journal of Periodontal Research Dec 2021Periodontitis is a chronic inflammatory condition that destroys the tooth-supporting tissues and eventually leads to tooth loss. As one of the most prevalent oral... (Review)
Review
Periodontitis is a chronic inflammatory condition that destroys the tooth-supporting tissues and eventually leads to tooth loss. As one of the most prevalent oral conditions, periodontitis endangers the oral health of 70% of people throughout the world. Periodontitis is also related to various systemic diseases, such as diabetes mellitus, atherosclerosis, and rheumatoid arthritis, which not only has a great impact on population health status and the quality of life but also increases the social burden. Porphyromonas gingivalis (P. gingivalis) is a gram-negative oral anaerobic bacterium that plays a key role in the pathogenesis of periodontitis. Porphyromonas gingivalis can express various of virulence factors to overturn innate and adaptive immunities, which makes P. gingivalis survive and propagate in the host, destroy periodontal tissues, and have connection to systemic diseases. Porphyromonas gingivalis can invade into and survive in host tissues by destructing the gingival epithelial barrier, internalizing into the epithelial cells, and enhancing autophagy in epithelial cells. Deregulation of complement system, degradation of antibacterial peptides, and destruction of phagocyte functions facilitate the evasion of P. gingivalis. Porphyromonas gingivalis can also suppress adaptive immunity, which allows P. gingivalis to exist in the host tissues and cause the inflammatory response persistently. Here, we review studies devoted to understanding the strategies utilized by P. gingivalis to escape host immunity. Methods for impairing P. gingivalis immune evasion are also mentioned.
Topics: Base Composition; Humans; Immune Evasion; Phylogeny; Porphyromonas gingivalis; Quality of Life; RNA, Ribosomal, 16S; Sequence Analysis, DNA
PubMed: 34254681
DOI: 10.1111/jre.12915 -
Molecular Oral Microbiology Aug 2021RagA and RagB proteins are major components of the outer membrane of the oral pathogen Porphyromonas gingivalis and, while recently suggested to represent a novel... (Review)
Review
RagA and RagB proteins are major components of the outer membrane of the oral pathogen Porphyromonas gingivalis and, while recently suggested to represent a novel peptide uptake system, their full function is still under investigation. Herein, we (a) discuss the evidence that the rag locus contributes to P. gingivalis virulence; (b) provide insight to Rag protein potential biological function in macromolecular transport and other aspects of bacterial physiology; (c) address the host response to Rag proteins which are immunodominant and immunomodulatory; and (d) review the potential of Rag-focused therapeutic strategies for the control of periodontal diseases.
Topics: Bacterial Proteins; Humans; Periodontal Diseases; Porphyromonas gingivalis; Virulence
PubMed: 34032024
DOI: 10.1111/omi.12345 -
Journal of Leukocyte Biology Oct 2020Discussion on the identification of an osteoclast precursor population, which emerges in the bone marrow after systemic infection with a periodontal pathogen.
Discussion on the identification of an osteoclast precursor population, which emerges in the bone marrow after systemic infection with a periodontal pathogen.
Topics: Osteoclasts; Porphyromonas gingivalis
PubMed: 33405332
DOI: 10.1002/JLB.3CE0720-364R -
Frontiers in Immunology 2023Atherosclerosis (AS) is a chronic inflammatory disease, involving a pathological process of endothelial dysfunction, lipid deposition, plaque rupture, and arterial... (Review)
Review
Atherosclerosis (AS) is a chronic inflammatory disease, involving a pathological process of endothelial dysfunction, lipid deposition, plaque rupture, and arterial occlusion, and is one of the leading causes of death in the world population. The progression of AS is closely associated with several inflammatory diseases, among which periodontitis has been shown to increase the risk of AS. (), presenting in large numbers in subgingival plaque biofilms, is the "dominant flora" in periodontitis, and its multiple virulence factors are important in stimulating host immunity. Therefore, it is significant to elucidate the potential mechanism and association between and AS to prevent and treat AS. By summarizing the existing studies, we found that promotes the progression of AS through multiple immune pathways. can escape host immune clearance and, in various forms, circulate with blood and lymph and colonize arterial vessel walls, directly inducing local inflammation in blood vessels. It also induces the production of systemic inflammatory mediators and autoimmune antibodies, disrupts the serum lipid profile, and thus promotes the progression of AS. In this paper, we summarize the recent evidence (including clinical studies and animal studies) on the correlation between and AS, and describe the specific immune mechanisms by which promotes AS progression from three aspects (immune escape, blood circulation, and lymphatic circulation), providing new insights into the prevention and treatment of AS by suppressing periodontal pathogenic bacteria.
Topics: Animals; Porphyromonas gingivalis; Periodontitis; Inflammation; Atherosclerosis; Lipids
PubMed: 36999040
DOI: 10.3389/fimmu.2023.1103592 -
Applied Biochemistry and Biotechnology Jan 2023Periodontitis, being a multifactorial disorder is found to be the most common oral disease denoted by the inflammation of gingiva and resorption of tooth supporting... (Review)
Review
Periodontitis, being a multifactorial disorder is found to be the most common oral disease denoted by the inflammation of gingiva and resorption of tooth supporting alveolar bone. The disease being closely linked with fast life style and determined by unhygienic behavioural factors, the internal milieu of oral cavity and formation of plaque biofilm on the dental and gingival surfaces. Porphyromonas gingivalis, being the major keystone pathogen of the periodontal biofilm evokes host immune responses that causes damage of gingival tissues and resorption of bones. The biofilm associated microbial community progressively aggravates the condition resulting in chronic inflammation and finally tooth loss. The disease often maintains bidirectional relationship with different systemic, genetic, autoimmune, immunodeficiency diseases and even psychological disorders. The disease can be diagnosed and predicted by various genetic, radiographic and computer-aided design (CAD) & computer-aided engineering (CAE) and artificial neural network (ANN). The elucidation of genetic background explains the inheritance of the disease. The therapeutic approaches commonly followed include mechanical removal of dental plaque with the use of systemic antibiotics. Awareness generation amongst local people, adoption of good practice of timely tooth brushing preferably with fluoride paste or with nanoconjugate pastes will reduce the chance of periodontal plaque formation. Modern tissue engineering technology like 3D bioprinting of periodontal tissue may help in patient specific flawless regeneration of tooth structures and associated bones.
Topics: Humans; Periodontitis; Inflammation; Gingiva; Porphyromonas gingivalis; Anti-Bacterial Agents
PubMed: 36098930
DOI: 10.1007/s12010-022-04127-9 -
Best Practice & Research. Clinical... Apr 2015The relationship between rheumatoid arthritis and poor oral health has been recognised for many decades. The association between periodontal infection and the risk of... (Review)
Review
The relationship between rheumatoid arthritis and poor oral health has been recognised for many decades. The association between periodontal infection and the risk of developing RA has been the subject of epidemiological, clinical and basic science research in recent times. Converging and reproducible evidence now makes a clear case for the role of specific periodontal infective pathogens in initiating, amplifying and perpetuating rheumatoid arthritis. The unique enzymatic properties of the periodontal pathogen Porphyromonas gingivalis and its contribution to the burden of citrullinated peptides is now well established. The impact of localized infection such as periodontitis in shaping specific anti-citrullinated peptide immune responses highlights a key area for treatment, prevention and risk assessment in rheumatoid arthritis.
Topics: Arthritis, Rheumatoid; Bacteroidaceae Infections; Humans; Hydrolases; Periodontitis; Porphyromonas gingivalis; Protein-Arginine Deiminases
PubMed: 26362738
DOI: 10.1016/j.berh.2015.03.001 -
Cancer Prevention Research... Apr 2023Several periodontitis-associated species induce genes related to cell proliferation, cell-cycle progression, apoptosis, intracellular transport, immune and inflammatory... (Review)
Review
Several periodontitis-associated species induce genes related to cell proliferation, cell-cycle progression, apoptosis, intracellular transport, immune and inflammatory responses, carcinogenesis, and cancer progression. Here, we reviewed studies showing strong associations between gingival squamous cell carcinoma (GSCC) and three periodontitis-related oral bacteria (Porphyromonas gingivalis, Fusobacterium nucleatum, and Prevotella intermedia) in the microenvironment. These bacteria produce cytoplasmic lipopolysaccharide (LPS) and secrete cytokines and molecules related to carcinogenesis, tumor progression, and metastasis and metastasis. In GSCC, LPS levels are substantially elevated and assessable by functional analysis. Polymicrobial infections can synergistically induce inflammation and significantly upregulate proinflammatory molecules (e.g., IL1β, IL8, and TNFα) that promote carcinogenesis. This review can facilitate the identification of novel targets for treating and preventing GSCC, which is potentially associated with periodontal pathogen.
Topics: Humans; Lipopolysaccharides; Periodontitis; Porphyromonas gingivalis; Squamous Cell Carcinoma of Head and Neck; Head and Neck Neoplasms; Carcinogenesis; Tumor Microenvironment
PubMed: 36688805
DOI: 10.1158/1940-6207.CAPR-22-0511